Kidney disease symptoms
Kidney disease in the world today constitute one of the most serious problems.Many kidney disease can occur long time in a latent or abortive form.How to treat kidney disease folk remedies, see here.
In nephrology practice allocate a number of syndromes:
Some syndromes (eg, nephrotic, hypertensive) are deployed clinical picture of the disease when patients tend to have certain complaints and the many manifestations of the disease.For the diagnosis of other syndromes necessary to use special methods of investigation.
In some cases, these syndromes may be due to unilateral renal disease, simulating two-way process, so you must always be aware of asymmetric renal lesions.It should be borne in mind often ephemeral syndrome which may occur for the first time early in the disease, and then not be repeated (e.g., nephrotic syndrome).This possibility makes the study the history of the patient with great care, since the terms of the existence of one or another syndrome often determine the prognosis and tr
for Nephrology diagnosis of great importance is the identification of proteinuria and hematuria.
Proteinuria - important and most common symptom of kidney damage, which requires a thorough examination of the patient.Normally, the urinary excretion of protein in adults does not exceed 150 mg / day, and children up to 10 years - 100 mg / day.Sedimentary protein samples may give false-positive results in the presence in urine of iodine contrast media, a large amount of penicillin or cephalosporin analogs, metabolites sulfonamides.In the presence of severe leukocyturia especially hematuria positive reaction to the protein may be a consequence of the collapse of the formed elements of urine during prolonged standing.Urine using test strips reveals proteinuria only if protein excretion exceeds 0.3 g / l.Proteinuria over 3 g / day results in the development of nephrotic syndrome.In
urine in kidney diseases exhibit various plasma proteins - a low molecular weight (albumin, ceruloplasmin, transferrin, etc.), And high molecular weight (α2-macroglobulins, γ-globulins).Depending on the content of certain proteins in the plasma and urine emit selective and nonselective proteinuria (the term conditional, to speak about the selective isolation of protein fractions, the selectivity of their clearance).
addition of plasma proteins in the urine can be determined kidney origin proteins - mukoproteinov Tamm-Horsfall secreted by the epithelium of the convoluted tubules.
When proteinuria kidney disease often associated with increased filtration of plasma proteins through the glomerular capillaries - the so-called glomerular (glomerular) proteinuria.Filtration of plasma proteins through the wall of the capillaries depends on the structural and functional state of the glomerular capillary wall, the properties of protein molecules, pressure, and flow rate, determining GFR.
The wall of the glomerular capillary endothelial cells make up (with round holes between cells), three-layer basement membrane - hydrated gel, as well as epithelial cells (podocytes) braided "nozhkovyh" processes.Due to this complicated structure of the glomerular capillary wall can "sift" molecule from plasma capillaries in the glomerulus of the capsule, with the function of "molecular sieves" largely depends on the pressure and flow rate in capillaries.In pathological conditions, "then" sizes can increase immune complex deposits can cause local changes in the capillary wall, increasing its permeability to macromolecules.
addition to mechanical constraints ( 'long' sizes) are important and electrostatic factors.BMK is negatively charged;a negative charge, and bear the podocyte foot.Under normal conditions, the negative charge of the glomerular filter repels anions - negatively charged molecules (including molecules of albumin).Loss of negative charge helps albumin filtration.It is suggested that in the body of patients with glomerular minimal change disease and focal segmental glomerulosclerosis produced humoral factors constant, changing the charge of BMC and podocyte feet.It is believed that the merger nozhkovyh processes - morphological equivalent of the negative charge loss.
Glomerular proteinuria is observed in the majority of kidney disease - in glomerulonephritis, renal amyloidosis, diabetic glomerulosclerosis, renal vein thrombosis, as well as hypertension, atherosclerotic nephrosclerosis, "stagnant" kidney.
Tubular (tubular) proteinuria occurs rarely.It is related to the inability of the proximal tubule reabsorb plasma low molecular weight proteins, the filtered in normal glomeruli.Kanaltsievaya proteinuria rarely exceeds 2 g / day, protein is represented by albumin, as well as the fractions with even more low molecular weight (lysozyme (32 microglobules Mr. ribonuclease-free with light chain immunoglobulin), absent in healthy individuals and glomerular (glomerular) proteinuriain connection with a 100% reabsorption of the epithelium of the convoluted tubules characteristic feature tubular (tubular) proteinuria -.. the prevalence of P2-microglobulin of albumin, as well as the absence of high molecular weight proteins
tubular proteinuria is observed in lesions of the renal tubules and interstitial - interstitial nephritis, pyelonephritis, kaliypenicheskoykidney, acute tubular necrosis, chronic rejection of a kidney transplant, congenital tubulopathy.
overflow Proteinuria (Fanconi syndrome) develops when excessive formation of plasma low molecular weight proteins (light chains of immunoglobulins, hemoglobin, myoglobin), which are filtered by normal glomeruli in excess of the ability of the tubulesto reabsorption.This is the mechanism of proteinuria in multiple myeloma (Bence-Jones proteinuria, see the clinical analysis of the "Myeloma Bence-Jones with a" large "proteinuria" at the end of this section.), Myoglobinuria.An example of such proteinuria - lizotsimuriya described in patients with leukemia.
Differentiation types of proteinuria can be carried out only by determining the protein fractions in urine (biochemical and immunohistochemical methods).
In Bright's (non-system) and lupus glomerulonephritis, diabetic glomerulosclerosis, proteinuria is usually combined with the red blood cell;proteinuric pure form are rare.
for renal amyloidosis, renal vein thrombosis, as well as for hypertensive disease is more common isolated proteinuria (proteinuria or, combined with a low red blood cell).When hemorrhagic purpura Henoch-Shёnleyna, polyarteritis nodosa eritrotsiturii usually expressed more than proteinuria.
addition, proteinuria may have extrarenal origin - be the result of the disintegration of cells in diseases of the urinary tract or genitals, during prolonged standing urine (proteinuria false).
should bear in mind the possibility of a functional proteinuria, the exact mechanisms have not been established pathogenesis.These include orthostatic proteinuria, idiepaticheskuyu transient proteinuria, proteinuria voltage and feverish proteinuria.
For her typical appearance of protein in the urine during prolonged standing or walking with the rapid disappearance in the horizontal position.
proteinuria Feature: usually does not exceed 1 g / day, glomerular, non-selective, mechanism of its origin is not clear.More often observed in young adulthood, half of the patients disappear in 5-10 years.
diagnosis of orthostatic proteinuria put under the following criteria:
to confirm the diagnosis is necessary to orthostatic test.Urine was collected in the morning before the rise from the bed, and then - after a 1-2-hour stay in the upright position (walking, preferably with hyperlordosis with a stick behind his back to straighten the spine).The sample provides even more accurate results, if morning (night) urine sample is poured (as in the bladder may be residual urine), and the first portion going after 1- 2-hour stay in the horizontal position of the subject.
in adolescence can be seen as idiopatiches-Kuyu transient proteinuria, detectable in healthy persons in the rest of the medical examination and the lack of subsequent studies of urine.
voltage Proteinuria, detected in 20% of healthy individuals (including athletes) after a sharp physical exertion with the detection of the protein in the first portion of the collected urine, a tubular (tubular) character.
is believed that this mechanism of proteinuria is associated with redistribution of the blood flow of relative ischaemia and proximal and distal tubules.
feverish proteinuria observed in acute fevers, especially in children and elderly persons;it is predominantly glomerular character.The mechanisms of these types of proteinuria have been little studied.Suggests the possibility of enhancing the role of glomerular filtration along with the defeat of the glomerular filter transient immune complexes.
is important to establish the fact of proteinuria and the degree of its severity, as in most cases, proteinuria is one of the main signs of kidney damage.High
proteinuria - urinary protein excretion in an amount of more than 3 g / day, which often leads to the development of nephrotic syndrome.This type of proteinuria is observed in acute and chronic glomerulonephritis, kidney disease in systemic diseases (lupus, hemorrhagic vasculitis, etc.) With renal amyloidosis, subacute infective endocarditis.Proteinuria can also be observed in multiple myeloma, and renal vein thrombosis, as well as diabetic nephropathy.
moderate proteinuria - urinary protein excretion in an amount of 0.5 to 3 g / day;it is observed in all of the above diseases and malignant hypertension, periarteritis nodosa, hypertension, renal vascular arteriosclerosis (ischemic kidney disease) and other diseases.
excretion of albumin in the urine (microalbuminuria) appears before other signs of kidney disorders that can be set currently available methods, and reflects the loss of renal microvascular bed (and also other vascular areas - heart, brain).The diagnostic value of microalbuminuria is as follows.Firstly, it is the earliest indicator of renal disease in patients with diabetes type I and II and in hypertensive patients;so she identifies prognostically most heavy group, which requires close monitoring with tight control of glucose levels in the blood and blood pressure.Secondly, the appearance of microalbuminuria predicts adverse outcome of cardiovascular disease (myocardial infarction, stroke), especially in patients with so-called high-risk groups - have diabetes, obesity, hypertension or a family history of vascular and renal diseases.
In recent years, there are more data on the "toxic" effect of proteinuria.It is found that the plasma proteins passing through the membrane in the glomerular nephropathy, represent not only a reliable marker of kidney damage, but also a factor damaging the structure of actively renal tissue inflammation and enhancing inducing fibrosis primarily tubulointerstitial.
Attention to proteinuria as an important factor in the progression of renal parenchymal disease increased especially after the establishment of a direct link between the magnitude of proteinuria and the risk of progression of renal failure, to a lesser extent depending on the morphology of the renal process.
has long been known for the fact of tubulointerstitial inflammation along with glomerular patients with proteinuric forms of nephritis.However, until recently it was not clear whether this is a consequence of coronary obliteration peri-tubular capillary or albumin and other proteins that accumulate in the lumen of the renal tubules, can actually cause inflammation interstitial.In recent years, it managed to prove that the severity and duration of proteinuria has at tubule epithelium toxicity.Intensive proximal tubule reabsorption epithelium of large amounts of filtered protein leads to the activation of skin cells and gene expression vasoactive and inflammatory substances.The molecules of these substances are produced by the renal tubules in excessive amounts, secreted through the basal cells in the interstitium, leading to the development of the inflammatory response, which in most forms of jade preceded by the development of renal scarring.
hematuria (blood in the urine) - frequent, often the first sign of kidney disease and urinary tract as well as diseases and conditions that are not associated with kidney disease (acute leukemia, thrombocytopenia, overdose of anticoagulants, heavy physical exertion, etc.).
hematuria with nephropathy (renal hematuria) are usually persistent bilateral painless, often combined with proteinuria, cylindruria, leukocyturia.Nevertheless, described form of glomerulonephritis occurring with recurrent isolated painful gross hematuria.
pathogenesis of renal hematuria is not entirely clear.It is believed that it was important mesangial involvement, as well as the defeat of the interstitial tissue and the epithelium of the convoluted tubules, as the most significant hematuria observed with mesangial nephritis and interstitial nephritis.Hematuria can be caused by necrotizing inflammation of the renal arterioles, renal intravascular coagulation, renal infarction.
by Japanese authors in the series of electron diffraction has been recently shown that red blood cells can penetrate even through the smallest gaps BMC, changing the formu.Istinnuyu its gross hematuria should be distinguished from the false.Unlike true, false haematuria due to urinary staining red are not erythrocytes, and other substances.
Renal hematuria observed with AGN, CGN, as well as many nephropathy occurring against the background of systemic diseases.
Ostronefritichesky syndrome manifests hematuria, proteinuria (more moderate), edema, hypertension .. However, currently most acute nephritis is atypical, and a number of symptoms, including a massive hematuria, may be missing.Recurrent ostronefriticheskim syndrome often manifests mesangioproliferative CGN variant, characterized by acute nephritis morphological picture.
One of the most common causes of isolated hematuria - IgA-nephropathy or Berger's disease (focal mesangial nephritis).IgA-nephropathy identify, as a rule, in children and adults under the age of 30 years, more common in men;gross hematuria manifested bouts (less persistent microscopic haematuria), with dull pain in the back, against the background of recurrent pharyngitis.Proteinuria is usually minimal.The disease in children is usually benign in adults worse prognosis.
This hematuric IgA-nephritis with increased IgA concentration in serum is characteristic of patients with chronic alcoholism.It is detected mainly in persons over 40 years on the background of alcoholic liver disease in combination with other systemic symptoms of alcoholism (lesions of the pancreas, heart, polyneuropathy).Unlike Berger disease "alcoholic" glomerulonephritis appears resistant microhematuria painless and takes a heavy - often joined by hypertension, rapidly developing renal insufficiency.
hematuria - a characteristic feature of interstitial nephritis, including acute drug.The reason may be hematuria variety of drugs, most commonly sulfonamides, streptomycin, kanamycin, gentamicin, analgesics (phenacetin, analgin) pirazolidonovye derivatives (phenylbutazone), and salts of heavy metals.
describes a special version of the pain hematuric nephropathy - lyumbalgicheski-hematuric syndrome occurs mainly in young women who use oral contraceptives estrogensoderzhaschie but described isolated cases of the disease in men.Art.Art.Art.Art.